MESO-Rx
Anabolic Steroids
My (Not So Good) Experience With TMG
- Thread starter DavidZ
- Start date
But there is DIM and then there is Indolplex/DIM guys taking reg. DIM are finding that if they take it with oil it works better. Indolplex/DIM is different and the stomach does not effect the power of the DIM none of it is killed in the stomach. We are thinking the Indolplex in the DIM we are taking dose not work good with TMG.SWALE said:
http://www.ritecare.com/prodsheets/PHY-15336.html
Both David and I take this and adding TMG caused problems with higher E2. Yet my Total E came down my E2 went up and I am taking .5 mg of Arimidex a day to keep it down. Also my DHT went up over 2000.
A simple Medline search will yield numerous articles about the anti-cancer powers of diindolylmethane (DIM). The claim that DIM is pro-cancer flies against all of the literature on the topic.
One example of many is shown below.
***********************************************
Br J Cancer. 2004 Oct 4;91(7):1358-63.
Induction of apoptosis in human prostate cancer cell line, PC3, by 3,3'-diindolylmethane through the mitochondrial pathway.
Nachshon-Kedmi M, Yannai S, Fares FA.
Faculty of Food Engineering and Biotechnology, Technion-Israel Institute of Technology, Haifa 32000, Israel.
Prostate cancer is the most common malignancy and the second leading cause of male death in Western countries. Prostate cancer mortality results from metastases to the bones and lymph nodes and progression from androgen-dependent to androgen-independent disease. Although androgen ablation was found to be effective in treating androgen-dependent prostate cancer, no effective life-prolonging therapy is available for androgen-independent cancer. Epidemiological studies have shown a strong correlation between consumption of cruciferous vegetables and a lower risk of prostate cancer. These vegetables contain glucosinolates, which during metabolism give rise to several breakdown products, mainly indole-3-carbinol (I3C), which may be condensed to polymeric products, especially 3,3'-diindolylmethane (DIM). It was previously shown that these indole derivatives have significant inhibitory effects in several human cancer cell lines, which are exerted through induction of apoptosis. We have previously reported that I3C and DIM induce apoptosis in prostate cancer cell lines through p53-, bax-, bcl-2- and fasL-independent pathways. The objective of this study was examination of the apoptotic pathways that may be involved in the effect of DIM in the androgen-independent prostate cancer cell line, PC3, in vitro. Our results suggest that DIM induces apoptosis in PC3 cells, through the mitochondrial pathway, which involves the translocation of cytochrome c from the mitochondria to the cytosol and the activation of initiator caspase, 9, and effector caspases, 3 and 6, leading to poly ADP-ribose polymerase (PARP) cleavage and induction of apoptosis. Our findings may lead to the development of new therapeutic strategies for the treatment of androgen-independent prostate cancer.
PMID: 15328526 [PubMed - indexed for MEDLINE]
One example of many is shown below.
***********************************************
Br J Cancer. 2004 Oct 4;91(7):1358-63.
Induction of apoptosis in human prostate cancer cell line, PC3, by 3,3'-diindolylmethane through the mitochondrial pathway.
Nachshon-Kedmi M, Yannai S, Fares FA.
Faculty of Food Engineering and Biotechnology, Technion-Israel Institute of Technology, Haifa 32000, Israel.
Prostate cancer is the most common malignancy and the second leading cause of male death in Western countries. Prostate cancer mortality results from metastases to the bones and lymph nodes and progression from androgen-dependent to androgen-independent disease. Although androgen ablation was found to be effective in treating androgen-dependent prostate cancer, no effective life-prolonging therapy is available for androgen-independent cancer. Epidemiological studies have shown a strong correlation between consumption of cruciferous vegetables and a lower risk of prostate cancer. These vegetables contain glucosinolates, which during metabolism give rise to several breakdown products, mainly indole-3-carbinol (I3C), which may be condensed to polymeric products, especially 3,3'-diindolylmethane (DIM). It was previously shown that these indole derivatives have significant inhibitory effects in several human cancer cell lines, which are exerted through induction of apoptosis. We have previously reported that I3C and DIM induce apoptosis in prostate cancer cell lines through p53-, bax-, bcl-2- and fasL-independent pathways. The objective of this study was examination of the apoptotic pathways that may be involved in the effect of DIM in the androgen-independent prostate cancer cell line, PC3, in vitro. Our results suggest that DIM induces apoptosis in PC3 cells, through the mitochondrial pathway, which involves the translocation of cytochrome c from the mitochondria to the cytosol and the activation of initiator caspase, 9, and effector caspases, 3 and 6, leading to poly ADP-ribose polymerase (PARP) cleavage and induction of apoptosis. Our findings may lead to the development of new therapeutic strategies for the treatment of androgen-independent prostate cancer.
PMID: 15328526 [PubMed - indexed for MEDLINE]
ciobl
New Member
cpeil2 said:
apoptosis :a genetically determined process of cell self-destruction that is marked by the fragmentation of nuclear DNA, is activated either by the presence of a stimulus or by the removal of a stimulus or suppressing agent, is a normal physiological process eliminating DNA-damaged, superfluous, or unwanted cells (as immune cells targeted against the self in the development of self-tolerance or larval cells in amphibians undergoing metamorphosis), and when halted (as by genetic mutation) may result in uncontrolled cell growth and tumor formationcalled also programmed cell death.
a type of cell death in which the cell uses specialized cellular machinery to kill itself; a cell suicide mechanism that enables metazoans to control cell number and eliminate cells that threaten the animal's survival
Disintegration of cells into membrane-bound particles that are then eliminated by phagocytosis or by shedding.
True. But it has everything to do with the proven anti-cancer effects of DIM and, therefore, gives some perspective to the discussion.cpeil2 said:
To add even more perspective, a lot of researchers believe that elevated E2 is extremely harmful to the prostate and may even be the primary culprit in the development of prostate cancer.
The bottom line question is -- how do we best control E2?
ciobl
New Member
cpeil2 said:
cpeil, I understand your observation bro, but we are running in circles here
he came up with that article from Medline after Dr Crisler comments about the numerous estrogens and chemicals inducing cancer.
2-hydroxyestrone and 2-hydroxyestradiol offer protection against 16-hydroxyestrone .
the cyp1a1 enzyme that catalyzes 2-hydroxyestrone formation is inducible by indole-2-carbinol or diindolylmethane as well as omega -3 fatty acids.
thanks bro
frankwhardy
New Member
cpeil2 said:
I also couldn't find anything when I researched this issue previously. See this thread entitled "Is TMG really necessary when using DIM?":
https://thinksteroids.com/community/threads/134237895
Making the statement that what I wrote "flies in the face of all we know" is unwarranted. We have not seen "all the studies" on the subject here, or anywhere. Maybe someone can find them. I have seen two such studies which showed that DIM stimulated not only the CYP1A1 enzyme, thus increasing 2-OHE, but also the CYP1B1, which is why 4-OHE concentrations rise as well. TMG, or its child, DMG, provides methyl groups, thus helping wash the 4-OHE downstream. IF (and it's a big IF) this is true, in vivo, DIM should not be taken without a methyl donor, and would be especially dangerous in someone with a COMT enzyme deficiency.
The answer to the question "how do we best control estrogen" is an easy one. First, to decrease its overall concentration through an aromatase inhibitor. Then, by controlling its metabolites thorugh these various OTC products.
What exactly is "Indolplex"?
The answer to the question "how do we best control estrogen" is an easy one. First, to decrease its overall concentration through an aromatase inhibitor. Then, by controlling its metabolites thorugh these various OTC products.
What exactly is "Indolplex"?
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Maybe this has some significance. Three months ago I had the battery of tests done while on the following:
1) .5ml 10% compounded t cream
2) 525iu hcg
3) 35mg zinc
4) 25mg dhea
5) Indoplex DIM with TMG
6) 1 Grain Armour
Results were as follows:
Total T: 616 (range 241-827)
Free T: 18 (Don't know, but 20something being upper limit)
E2: 35 (10-54)
TSH: .03 (.35-5.5)
Last Wednesday I was tested again, only I was on:
1) 1ml 10% compounded test cream
2) 455iu hcg
3) 65mg zinc
4) 50mg dhea
5) 1/2 grain armour and 25mcg synthroid
Results were as follows and same ranges apply:
Total T: 1689
Free T: 43.2
E2: 31
TSH: .004
My T/E ratio went from less than 20:1 to 54:1 and the only thing I changed was zinc, DHEA and HCG. Obviously I need to lower my total T, free T, and thyroid dosages but I thought my T/E ratio was interesting. Still waiting for DHT but since I went to 1ml I've been on 1mg proscar eod. Interesting that my total and free t went up that much while being on proscar. Sex drive still there as well
1) .5ml 10% compounded t cream
2) 525iu hcg
3) 35mg zinc
4) 25mg dhea
5) Indoplex DIM with TMG
6) 1 Grain Armour
Results were as follows:
Total T: 616 (range 241-827)
Free T: 18 (Don't know, but 20something being upper limit)
E2: 35 (10-54)
TSH: .03 (.35-5.5)
Last Wednesday I was tested again, only I was on:
1) 1ml 10% compounded test cream
2) 455iu hcg
3) 65mg zinc
4) 50mg dhea
5) 1/2 grain armour and 25mcg synthroid
Results were as follows and same ranges apply:
Total T: 1689
Free T: 43.2
E2: 31
TSH: .004
My T/E ratio went from less than 20:1 to 54:1 and the only thing I changed was zinc, DHEA and HCG. Obviously I need to lower my total T, free T, and thyroid dosages but I thought my T/E ratio was interesting. Still waiting for DHT but since I went to 1ml I've been on 1mg proscar eod. Interesting that my total and free t went up that much while being on proscar. Sex drive still there as well
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ciobl said:cpeil, I understand your observation bro, but we are running in circles here
he came up with that article from Medline after Dr Crisler comments about the numerous estrogens and chemicals inducing cancer.
2-hydroxyestrone and 2-hydroxyestradiol offer protection against 16-hydroxyestrone .
the cyp1a1 enzyme that catalyzes 2-hydroxyestrone formation is inducible by indole-2-carbinol or diindolylmethane as well as omega -3 fatty acids.
thanks bro
That's the bridge I was looking for. Thanks. I'm lazy. If possible, I like to let others deconstruct biochemical pathways.
SWALE said:
I remember we had this discussion months back. I found this post from Jboldman:
https://thinksteroids.com/community/posts/413264
cpeil2 said:
But, then I just found this:
Ann N Y Acad Sci. 1999;889:204-13.
Multifunctional aspects of the action of indole-3-carbinol as an antitumor agent.
Bradlow HL, Sepkovic DW, Telang NT, Osborne MP.
Strang Cancer Research Laboratory, New York, New York 10021, USA. leon@rockvax.rockefeller.edu
Previous studies from this laboratory have suggested that 2-hydroxyestrone is protective against breast cancer, whereas the other principal metabolite, 16 alpha-hydroxyestrone, and the lesser metabolite quantitatively, 4-hydroxyestrone, are potent carcinogens. Attempts to directly decrease the formation of the 16-hydroxylated metabolite were either unsuccessful or required such high levels of the therapeutic agent as to be impractical. On the other hand the concentration of the protective metabolite, 2-hydroxyestrone, proved to be readily modulated by a variety of agents, both in the direction of increased protection and the opposite direction, increased risk by a variety of agents and activities. We have focussed our attention on indole-3-carbinol, a compound found in cruciferous vegetables, and its further metabolites in the body, diindolylmethane (DIM) and indolylcarbazole (ICZ), because of its relative safety and multifaceted activities. It has been shown that it induces CyP4501A1, increasing 2-hydroxylation of estrogens, leading to the protective 2-OHE1, and also decreases CyP1B1 sharply, inhibiting 4-hydroxylation of estradiol, thereby decreasing the formation of the carcinogenic 4-OHE1. In addition to these indirect effects as a result of altered estrogen metabolism, indole-3-carbinol has been shown to have direct effects on apoptosis and cyclin D, resulting in blockage of the cell cycle. In addition to its antitumor activity in animals, it has also been shown to be effective against HPV-mediated tumors in human patients. All of these responses make the study of its behavior as a therapeutic agent of considerable interest.
Publication Types:
* Review
* Review, Tutorial
PMID: 10668495 [PubMed - indexed for MEDLINE]
ciobl
New Member
We have focussed our attention on indole-3-carbinol, a compound found in cruciferous vegetables, and its further metabolites in the body, diindolylmethane (DIM) and indolylcarbazole (ICZ), because of its relative safety and multifaceted activities. It has been shown that it induces CyP4501A1, increasing 2-hydroxylation of estrogens, leading to the protective 2-OHE1, and also decreases CyP1B1 sharply, inhibiting 4-hydroxylation of estradiol, thereby decreasing the formation of the carcinogenic 4-OHE1.
cpeil that's the one !!
Dr Crisler said there are 2 studies showing an increase on cyp1b1. why would they do that ? contradicting themselves ?
thank you cpeil
cpeil that's the one !!
Dr Crisler said there are 2 studies showing an increase on cyp1b1. why would they do that ? contradicting themselves ?
thank you cpeil
